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CRH — TPH1

Text-mined interactions from Literome

Singh et al., Neurochem Int 1992 : Corticotropin releasing factor (CRF) infused bilaterally into the lateral ventricles of awake, chronically cannulated, male Sprague-Dawley rats produced a dose dependent increase in the in vitro activity of cortical and midbrain tryptophan hydroxylase after 60 min ... Intracerebroventricular administration of the glucocorticoid antagonist, RU 38486 ( 200 micrograms/day for 4 days ), also blocked the acute increase in tryptophan hydroxylase activity in response to CRF
Evans et al., Neurosci Lett 2009 : Corticotropin releasing factor (CRF) induced activation of a subset of serotonergic neurons in the caudal dorsal raphe nucleus ( DR ) may underlie stress related increases in TPH activity in the MnR and a mesolimbocortical serotonergic system ... To examine the effect of CRF receptor activation on TPH activity, freshly prepared brain slices were exposed to CRF ( 0-2000 nM ) for 10 min in the presence of NSD-1015, then frozen and microdissected for analysis of tissue 5-HTP concentrations
Boadle-Biber et al., Brain Res 1993 : The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase , the rate limiting enzyme in serotonin synthesis, produced in response to sound stress ... The activation of tryptophan hydroxylase , produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist alpha-helical CRF9-41 ( 10 micrograms ) ... Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons